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[Federal Register: February 26, 2010 (Volume 75, Number 38)]
[Proposed Rules]               
[Page 8889-8894]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr26fe10-21]                         

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[EPA-HQ-TRI-2009-0844; FRL-9119-2]
RIN 2025-AA27

 
Hydrogen Sulfide; Community Right-to-Know Toxic Chemical Release 
Reporting

AGENCY: Environmental Protection Agency (EPA).

ACTION: Intent to consider lifting administrative stay; opportunity for 
public comment.

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SUMMARY: EPA is announcing that it is considering whether to lift the 
Administrative Stay of the Emergency Planning and Community Right-to-
Know Act (EPCRA) section 313 toxic chemical release reporting 
requirements for hydrogen sulfide (Chemical Abstracts Service Number 
(CAS No.) 7783-06-4). Hydrogen sulfide was added to the EPCRA section 
313 list of toxic chemicals in a final rule published in the Federal 
Register on December 1, 1993. However, on August 22, 1994, EPA issued 
an Administrative Stay of the reporting requirements for hydrogen 
sulfide in order to evaluate issues brought to the Agency's attention 
after promulgation of the final rule concerning the human health effect 
basis for the listing and the Agency's use of exposure analysis in 
EPCRA section 313 listing decisions. Although the final rule listing 
hydrogen sulfide under section 313 of EPCRA remained in force, the stay 
deferred the reporting requirements for hydrogen sulfide while EPA 
completed this further evaluation. EPA has now completed its further 
evaluation, including a consideration of additional information that 
has become available since the stay was put in place regarding the 
human health and environmental effects of hydrogen sulfide. Based on 
this further evaluation, EPA believes that the Administrative Stay 
should be lifted. By this current action, EPA is not revisiting the 
original listing decision, which was accomplished by final rule on 
December 1, 1993. Rather, EPA is merely presenting its rationale for 
why the Administrative Stay of the reporting requirements for hydrogen 
sulfide should be lifted. After consideration of comments received, the 
Agency will issue another Federal Register document responding to 
comments and taking appropriate action.

DATES: Comments must be received on or before April 27, 2010.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
TRI-2009-0844, by one of the following methods:
    www.regulations.gov: Follow the on-line instructions for 
submitting comments.
     E-mail: oei.docket@epa.gov.
     Mail: Office of Environmental Information (OEI) Docket, 
Environmental Protection Agency, Mail Code: 28221T, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460
     Hand Delivery: EPA Docket Center (EPA/DC), EPA West, Room 
3334, 1301 Constitution Ave., NW., Washington, DC 20460. Such 
deliveries are only accepted during the Docket's normal hours of 
operation, and special arrangements should be made for deliveries of 
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-TRI-
2009-0844. EPA's policy is that all comments received will be included 
in the public docket without change and may be made available online at 
www.regulations.gov, including any personal information provided, 
unless the comment includes information claimed to be Confidential 
Business Information (CBI) or other information whose disclosure is 
restricted by statute. Do not submit information that you consider to 
be CBI or otherwise protected through www.regulations.gov or e-mail. 
The www.regulations.gov Web site is an ``anonymous access'' system, 
which means EPA will not know your identity or contact information 
unless you provide it in the body of your comment. If you send an e-
mail comment directly to EPA without going through www.regulations.gov, 
your e-mail address will be automatically captured and included as part 
of the comment that is placed in the public docket and made available 
on the Internet. If you submit an electronic comment, EPA recommends 
that you include your name and other contact information in the body of 
your comment and with any disk or CD-ROM you submit. If EPA cannot read 
your comment due to technical difficulties and cannot contact you for 
clarification, EPA may not be able to consider your comment. Electronic 
files should avoid the use of special characters, avoid any form of 
encryption, and be free of any defects or viruses.
    Docket: All documents in the docket are listed in the 
www.regulations.gov index. Although listed in the index, some 
information is not publicly available, e.g., CBI or other information 
whose disclosure is restricted by statute. Certain other material, such 
as copyrighted material, will be publicly

[[Page 8890]]

available only in hard copy. Publicly available docket materials are 
available either electronically in www.regulations.gov or in hard copy 
at the OEI Docket, EPA/DC, EPA West, Room 3334, 1301 Constitution Ave., 
NW., Washington, DC. This Docket Facility is open from 8:30 a.m. to 
4:30 p.m., Monday through Friday, excluding legal holidays. The 
telephone number for the Public Reading Room is (202) 566-1744, and the 
telephone number for the OEI Docket is (202) 566-1752.

FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Environmental 
Analysis Division, Office of Information Analysis and Access (2842T), 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460; telephone number: 202-566-0743; fax number: 202-
566-0677; e-mail: bushman.daniel@epa.gov, for specific information on 
this document. For general information on EPCRA section 313, contact 
the Emergency Planning and Community Right-to-Know Hotline, toll free 
at (800) 424-9346 or (703) 412-9810 in Virginia and Alaska or toll 
free, TDD (800) 553-7672, http://www.epa.gov/epaoswer/hotline/.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does This Action Apply to Me?

    You may be potentially affected by this action if you manufacture, 
process, or otherwise use hydrogen sulfide. Potentially affected 
categories and entities may include, but are not limited to:

------------------------------------------------------------------------
           Category            Examples of potentially affected entities
------------------------------------------------------------------------
Industry.....................  Facilities included in the following
                                NAICS manufacturing codes (corresponding
                                to SIC codes 20 through 39): 311*, 312*,
                                313*, 314*, 315*, 316, 321, 322, 323*,
                                324, 325*, 326*, 327, 331, 332, 333,
                                334*, 335*, 336, 337*, 339*, 111998*,
                                211112*, 212324*, 212325*, 212393*,
                                212399*, 488390*, 511110, 511120,
                                511130, 511140*, 511191, 511199, 512220,
                                512230*, 519130*, 541712*, or 811490*.
                               *Exceptions and/or limitations exist for
                                these NAICS codes.
                               Facilities included in the following
                                NAICS codes (corresponding to SIC codes
                                other than SIC codes 20 through 39):
                                212111, 212112, 212113 (correspond to
                                SIC 12, Coal Mining (except 1241)); or
                                212221, 212222, 212231, 212234, 212299
                                (correspond to SIC 10, Metal Mining
                                (except 1011, 1081, and 1094)); or
                                221111, 221112, 221113, 221119, 221121,
                                221122, 221330 (Limited to facilities
                                that combust coal and/or oil for the
                                purpose of generating power for
                                distribution in commerce) (correspond to
                                SIC 4911, 4931, and 4939, Electric
                                Utilities); or 424690, 425110, 425120
                                (Limited to facilities previously
                                classified in SIC 5169, Chemicals and
                                Allied Products, Not Elsewhere
                                Classified); or 424710 (corresponds to
                                SIC 5171, Petroleum Bulk Terminals and
                                Plants); or 562112 (Limited to
                                facilities primarily engaged in solvent
                                recovery services on a contract or fee
                                basis (previously classified under SIC
                                7389, Business Services, NEC)); or
                                562211, 562212, 562213, 562219, 562920
                                (Limited to facilities regulated under
                                the Resource Conservation and Recovery
                                Act, subtitle C, 42 U.S.C. 6921 et seq.)
                                (correspond to SIC 4953, Refuse
                                Systems).
Federal Government...........  Federal facilities.
------------------------------------------------------------------------

    This table is not intended to be exhaustive, but rather provides a 
guide for readers regarding entities likely to be affected by this 
action. Some of the entities listed in the table have exemptions and/or 
limitations regarding coverage, and other types of entities not listed 
in the table could also be affected. To determine whether your facility 
would be affected by this action, you should carefully examine the 
applicability criteria in part 372 subpart B of Title 40 of the Code of 
Federal Regulations. If you have questions regarding the applicability 
of this action to a particular entity, consult the person listed in the 
preceding FOR FURTHER INFORMATION CONTACT section.

B. How Should I Submit CBI to the Agency?

    Do not submit CBI information to EPA through www.regulations.gov or 
e-mail. Clearly mark the part or all of the information that you claim 
to be CBI. For CBI information in a disk or CD ROM that you mail to 
EPA, mark the outside of the disk or CD ROM as CBI and then identify 
electronically within the disk or CD ROM the specific information that 
is claimed as CBI. In addition to one complete version of the comment 
that includes information claimed as CBI, a copy of the comment that 
does not contain the information claimed as CBI must be submitted for 
inclusion in the public docket. Information so marked will not be 
disclosed except in accordance with procedures set forth in 40 CFR part 
2.

II. Introduction

    Section 313 of EPCRA, 42 U.S.C. 11023, requires certain facilities 
that manufacture, process, or otherwise use listed toxic chemicals in 
amounts above reporting threshold levels to report their environmental 
releases and other waste management quantities of such chemicals 
annually. These facilities must also report pollution prevention and 
recycling data for such chemicals, pursuant to section 6607 of the 
Pollution Prevention Act (PPA), 42 U.S.C. 13106. EPCRA section 313 
established an initial list of toxic chemicals composed of more than 
300 chemicals and 20 chemical categories.
    EPCRA section 313(d) authorizes EPA to add or delete chemicals from 
the list and sets forth criteria for these actions. Specifically, EPCRA 
section 313(d)(2) states that EPA may add a chemical to the list if 
``there is sufficient evidence to establish any one'' of the listing 
criteria. Therefore, to add a chemical, EPA must demonstrate that at 
least one criterion is met, but need not determine whether any other 
criterion is met. Conversely, EPCRA section 313(d)(3) states that to 
remove a chemical from the list, EPA must determine that ``there is not 
sufficient evidence to establish any'' of the Section 313(d)(2) 
criteria. Therefore, to remove a chemical, EPA must demonstrate that 
none of the criteria are met. The EPCRA section 313(d)(2) criteria are:

    (A) The chemical is known to cause or can reasonably be 
anticipated to cause significant adverse acute human health effects 
at concentration levels that are reasonably likely to exist beyond 
facility site boundaries as a result of continuous, or frequently 
recurring, releases.
    (B) The chemical is known to cause or can reasonably be 
anticipated to cause in humans--
    (i) Cancer or teratogenic effects, or
    (ii) Serious or irreversible--
    (I) Reproductive dysfunctions,
    (II) Neurological disorders,
    (III) Heritable genetic mutations, or
    (IV) Other chronic health effects.
    (C) The chemical is known to cause or can be reasonably 
anticipated to cause, because of
    (i) Its toxicity,
    (ii) Its toxicity and persistence in the environment, or
    (iii) Its toxicity and tendency to bioaccumulate in the 
environment, a significant adverse effect on the environment of 
sufficient seriousness, in the judgment of

[[Page 8891]]

the Administrator, to warrant reporting under this section.

EPA often refers to the section 313(d)(2)(A) criterion as the ``acute 
human health effects criterion;'' the section 313(d)(2)(B) criterion as 
the ``chronic human health effects criterion;'' and the section 
313(d)(2)(C) criterion as the ``environmental effects criterion.''
    Under EPCRA section 313(e)(1), any person may petition EPA to add 
chemicals to or delete chemicals from the list. EPA issued a statement 
of petition policy and guidance in the Federal Register of February 4, 
1987 (52 FR 3479) to provide guidance regarding the recommended content 
and format for submitting petitions under EPCRA section 313(e). EPA 
also issued guidance in the Federal Register of May 23, 1991 (56 FR 
23703) regarding the recommended content of petitions to delete 
individual members of the section 313 metal compound categories. In 
addition, EPA published in the Federal Register of November 30, 1994 
(59 FR 61432) a statement clarifying its interpretation of the section 
313(d)(2) and (d)(3) criteria for modifying the section 313 list of 
toxic chemicals.

III. Background Information

A. What is the History of the Listing of Hydrogen Sulfide Under EPCRA 
Section 313?

    In response to a petition from the Natural Resources Defense 
Council and the Governor of New York, hydrogen sulfide, along with 20 
other chemicals and two chemical categories, was added to the EPCRA 
section 313 list of toxic chemicals as part of a 1993 final rule 
(December 1, 1993, 58 FR 63500). Hydrogen sulfide was listed under the 
criteria of EPCRA section 313(d)(2)(B) (chronic human health effects) 
based on chronic neurotoxic effects in humans and under EPCRA section 
313(d)(2)(C) (environmental effects) based on acute aquatic toxicity. 
However, on August 22, 1994 (59 FR 43048), EPA issued an Administrative 
Stay of the EPCRA section 313 reporting requirements for hydrogen 
sulfide. Although the final rule listing hydrogen sulfide under section 
313 of EPCRA remained in force, the stay deferred the reporting 
requirements for hydrogen sulfide.

B. What Was the Basis for the Administrative Stay?

    After the final rule was issued adding hydrogen sulfide to the 
EPCRA section 313 list of toxic chemicals, some members of the 
regulated community expressed a concern that the ``chronic human health 
effects'' basis for listing hydrogen sulfide under EPCRA section 
313(d)(2)(B) changed between the proposed rule (September 8, 1992, 57 
FR 41020) and the final rule (December 1, 1993, 58 FR 63500), and that 
commenters on the proposed rule therefore did not have an opportunity 
to comment on that individual basis for the listing. Specifically, 
although the Agency cited the same acute aquatic toxicity as an 
``environmental effects'' basis for the listing under EPCRA section 
313(d)(2)(C) in both the proposed and final rules, the Agency also 
cited chronic respiratory effects as a ``chronic human health effects'' 
basis under EPCRA section 313(d)(2)(B) in the proposed rule, but 
chronic neurotoxic effects as a ``chronic human health effects'' basis 
under that same provision in the final rule. In addition, after 
issuance of the final rule, some members of the regulated community 
expressed concern that EPA's decision not to include an exposure 
analysis in deciding to list hydrogen sulfide on the basis of chronic 
human health effects was inconsistent with past Agency practice.
    Although EPA did not agree that it had been inconsistent in its use 
of exposure analyses, and notwithstanding the fact that the listing 
decision was dictated by the acute aquatic toxicity finding alone under 
EPCRA section 313(d)(2)(C), the Agency issued an Administrative Stay of 
the reporting requirements for hydrogen sulfide in order to review the 
concerns raised after issuance of the final rule by some members of the 
regulated community.

C. What Is the Purpose of This Document?

    The purpose of this document is to provide the public with the 
opportunity to comment on EPA's review of the currently available data 
on the human health and environmental effects of hydrogen sulfide--
specifically, chronic respiratory effects, chronic neurotoxic effects, 
and acute, chronic and early-life stage aquatic toxicity--and EPA's 
belief that the Administrative Stay should be lifted based on that 
data. EPA's analysis of the toxicity of hydrogen sulfide is based on 
the Agency's latest Toxicological Review of Hydrogen Sulfide (Ref. 1), 
as well as a reassessment of the environmental effects of hydrogen 
sulfide (Ref. 2). These assessments are discussed in detail in Unit IV. 
of this document. In addition, this document addresses the concerns 
raised regarding use of exposure analyses. After consideration of 
comments received, the Agency will issue another Federal Register 
document responding to comments and taking appropriate action.

IV. What Is EPA's Technical Review of Hydrogen Sulfide?

A. What Is EPA's Evaluation of the Human Health Toxicity of Hydrogen 
Sulfide?

    The following assessment of the human health toxicity of hydrogen 
sulfide is based on the information contained in EPA's most recent 
(June 2003) Integrated Risk Information System (IRIS) Toxicological 
Review of Hydrogen Sulfide (Ref. 1).
    Hydrogen sulfide is a colorless, acutely toxic gas at high 
concentrations. Hydrogen sulfide gas is absorbed rapidly through the 
lungs and can be absorbed through the gastrointestinal tract. Oral 
exposure is not likely to occur. In animals and humans, it distributes 
to the blood, brain, lungs, heart, liver, spleen, and kidneys. 
Oxidation is the primary metabolic pathway for hydrogen sulfide, with 
thiosulfate and sulfate as metabolites. Metabolism in laboratory 
animals and in humans appears to be similar. Hydrogen sulfide 
metabolites are excreted in the urine.
    A considerable body of case studies exists on the human health 
impacts resulting from acute exposure to high levels of hydrogen 
sulfide. Levels in the range of 500 to 1,000 parts per million (ppm) 
(695 to 1,390 milligrams per cubic meter (mg/m\3\)) are life-
threatening and can cause immediate unconsciousness followed by serious 
and debilitating neurologic and respiratory sequelae and death (Ref. 
1). While complete recovery from a high exposure episode has been 
reported, more often long term or even irreversible harmful 
neurological effects remain. Several groups of investigators (Tvedt, et 
al. (Refs. 3 and 4); Wasch, et al. (Ref. 5)) have reported long-term 
persistent adverse neurological effects from hydrogen sulfide-induced 
unconsciousness in humans during occupational, accidental, and chronic 
exposures, including neuropsychological and neurobehavorial decrements 
and brain damage. These irreversible effects are believed to be caused 
by an essentially hypoxic (low oxygen) condition existing in persons 
who become unconscious from a high exposure to hydrogen sulfide. 
Because a loss of oxygen (anoxia) utilization in tissues, particularly 
the brain, occurs in such poisonings, it is possible to attribute 
persistent neuronal damage to this effect. Permanent (chronic) damage 
is commonly observed clinically when

[[Page 8892]]

brain tissues have been deprived of oxygen due to inadequate delivery 
of the gas or to interrupted utilization of oxygen by cells, as is the 
case with hydrogen sulfide poisoning.
    The observed nonirritant effects produced in mammals from exposure 
to hydrogen sulfide gas may primarily be attributed to the cellular 
anoxia produced by inhibition of cytochrome oxidase (Ref. 1). 
Inhibition of cytochrome oxidase reduces the oxygen dependent 
metabolism of the cell, reduces cell energy sources (e.g., adenosine 
triphosphate (ATP)), increases products of anaerobic metabolism such as 
lactic acid, and produces cell death. Hence, cells with a high oxygen 
demand such as those in brain and cardiac tissue are thought to be more 
sensitive to disruption of oxidative metabolism and may be considered 
selected targets for the toxicity of hydrogen sulfide.
    1. Chronic Toxicity. EPA has reviewed the available toxicological 
studies on hydrogen sulfide in its most recent IRIS Toxicological 
Review of Hydrogen Sulfide (Ref. 1) and concluded that hydrogen sulfide 
can cause chronic human health toxicity. As reported in IRIS, the upper 
respiratory tract (neuronal and basal cells of the olfactory nasal 
epithelium) and neurologic tissues are both targets for hydrogen 
sulfide toxicity. The weight-of-evidence from the animal studies 
indicates that nasal tract lesions and neurological effects of hydrogen 
sulfide are dose-dependent, and both effects are clearly of relevance 
to humans. The levels of hydrogen sulfide associated with these effects 
appear to be similar for either endpoint (e.g., the no-effect level of 
nasal tract lesions reported by Brenneman, et al. (Ref. 6) at 10 ppm 
(14 mg/m\3\) and the likely indicator of neurotoxic effects reported by 
Hannah and Roth (Ref. 7) at 20 ppm (28 mg/m\3\)), which is some 
indication that consideration for one effect will also address the 
other (Ref. 1).
    a. Upper Respiratory Tract Toxicity. Several subchronic exposure 
studies in rats and mice indicate that low concentrations of hydrogen 
sulfide cause nasal lesions of the olfactory mucosa (Brenneman, et al. 
(Ref. 6); Dorman, et al. (Ref. 8); Chemical Industry Institute of 
Toxicology (Ref. 9); Lopez, et al. (Ref. 10); Dorman, et al. (Ref. 
11)). The nasal lesions are consistent with the neurotoxic and irritant 
properties of this gas. Based on the demonstrable histopathology, 
information available on exposure-dose-response, and the commonality of 
the underlying mechanism (cytochrome oxidase inhibition and irritation) 
between animals and humans, there is compelling indication that such 
effects are reasonably anticipated to occur in humans chronically 
exposed to hydrogen sulfide (Hirsch and Zavala (Ref. 12)).
    Brenneman, et al. (Ref. 6) reported significant concentration-
related increases in the incidence and severity of lesions to the nasal 
olfactory epithelium in rats exposed to 0, 10, 30, or 80 ppm of 
hydrogen sulfide for 10 weeks. The effects consisted of olfactory 
neuron loss and basal cell hyperplasia in rats exposed to 30 or 80 ppm, 
6 hours/day, 7 days/week for 10 weeks; no adverse effects were observed 
at 10 ppm. The severity of the olfactory neuron loss was concentration-
related; however, an inverse relationship between severity and 
concentration was observed for the basal cell hyperplasia suggesting 
that as the concentration increased, the ability of the olfactory 
epithelium to regenerate decreased. In contrast, earlier studies 
conducted by the Chemical Industry Institute of Toxicology (CIIT) 
(Refs. 13 and 14) where rats and mice were exposed to 0, 10.1, 30.5, or 
80 ppm of hydrogen sulfide, 6 hours/day, 5 days/week for 13 weeks, did 
not find significant alterations in the nasal turbinates of Fischer-344 
(F-344) or Sprague-Dawley rats exposed to 80 ppm or less of hydrogen 
sulfide. Inflammation of the squamous portion of the nasal mucosa was 
observed in mice exposed to 80 ppm hydrogen sulfide, 6 hours/day, 5 
days/week for 13 weeks (CIIT (Ref. 9)); the no-observed-adverse-effect-
level (NOAEL) for this effect is 30.5 ppm. However, a re-examination of 
the histological specimens from this study revealed a statistically 
significant increase in the incidence of olfactory neuron loss in 
Sprague-Dawley rats, F-344 rats, and B6C3F1 mice exposed to 30 or 80 
ppm; no lesions were observed at 10 ppm (Dorman, et al. (Ref. 11)). In 
addition, increases in the incidence of bronchiolar epithelial 
hyperplasia and hypertrophy were observed in female Sprague-Dawley rats 
exposed to 30 or 80 ppm and male Sprague-Dawley and F-344 rats exposed 
to 80 ppm.
    b. Neurotoxicity. The neurotoxic effects of low level hydrogen 
sulfide exposure have been primarily assessed from neurodevelopmental 
toxicity studies. Male Sprague-Dawley rats and male B6C3F1 mice exposed 
to 80 ppm of hydrogen sulfide (6 hours/day, 5 days/week for 13 weeks) 
had a statistically significant decrease in absolute (but not relative) 
brain weight (CIIT (Ref. 13) and Dorman, et al. (Ref. 11)) at 80 ppm 
but not 30 ppm. In an earlier study, Skrajny, et al. (Ref. 15) examined 
the effect of hydrogen sulfide exposure on serotonin and norepinephrine 
levels in the developing cerebellum and frontal cortex of Sprague-
Dawley rats. Timed-pregnant rats were exposed to 0, 20 or 75 ppm for 7 
hours/day from gestational day 5 until post natal day (PND) 21. There 
were statistically significant increases in serotonin levels in the 
frontal cortex on PND 21 in pups exposed to 20 ppm hydrogen sulfide and 
increases in serotonin levels in the cerebellum and frontal cortex on 
postpartum days 14 and 21 in pups exposed to 75 ppm hydrogen sulfide. 
Norepinephrine levels were increased at 75 ppm in the cerebellum on 
PNDs 7, 14, and 21, and in the frontal cortex on PND 21. At 20 ppm 
frontal cortex norepinephrine levels were decreased compared to 
controls on days 14 and 21.
    In a similarly designed study using the same exposure protocol as 
the CIIT (Refs. 9, 13, and 14) and Dorman, et al. (Ref. 11) studies, 
Hannah and Roth (Ref. 7) evaluated the perinatal effect of hydrogen 
sulfide on developing cerebellar Purkinje cells. Sprague-Dawley dams 
were exposed to 0, 20 or 50 ppm hydrogen sulfide for 7 hr/day from 
gestational day 5 until PND 21. Exposure to both 20 and 50 ppm 
interrupted normal dendritic growth of Purkinje cells in the brain of 
offspring. In later studies using this same experimental protocol, 
Hannah, et al. (Refs. 16 and 17) also found decreases in several brain 
amino acid levels in Sprague-Dawley rats exposed to 75 ppm of hydrogen 
sulfide.
    The significance of the morphological changes and alteration of 
brain neurotransmitters in these studies and the Skrajny, et al. (Ref. 
15) study to humans is unclear. Since Purkinje cell alterations and 
changes in neurotransmitter levels may constitute a hydrogen sulfide-
induced change in the growth or organization of structural (or 
neurochemical) elements, they are to be regarded as indicators of a 
neurotoxic effect in accordance with guidance in EPA's neurotoxicity 
risk assessment guidelines (Ref. 18). The question as to what 
functional impairment these alterations might lead to in humans remains 
unclear. Predicting particular functional impairments from decreased 
brain weight and specific structural alterations such as reported by 
the CIIT (Refs. 9, 13, and 14) and Dorman, et al. (Ref. 11) studies and 
Hannah and Roth (Ref. 7) is difficult due to the selective nature of 
the observed alterations and the dynamic self-organizing response of 
the developing brain to injury. Although behavioral testing has not 
indicated that alterations of brain neurotransmittters

[[Page 8893]]

have a functional impact (Dorman, et al. (Ref. 8)), further examination 
of the biochemical and functional aspects of the developing brain in 
hydrogen sulfide-exposed animals is warranted and neurotoxic effects 
cannot be discounted.
    Available information indicates that the dose-response character of 
indicators of neurotoxicity (such as the alterations to cerebellar 
Purkinje cells reported by Hannah and Roth (Ref. 7) and nasal olfactory 
(neuronal cell) lesions reported by Brenneman, et al. (Ref. 6)) may be 
similar to one another, such that consideration of one may be inclusive 
of the other. However, more extensive and definitive information on the 
neurologic endpoints could reveal that these should be the most 
relevant endpoints, more so than nasal tract lesions. The IRIS Summary 
for Hydrogen Sulfide (Ref. 1) indicates that such information may 
provide sufficient reason to reassess hydrogen sulfide.
    2. Summary. As stated in the IRIS Summary for Hydrogen Sulfide 
(Ref. 1) and as discussed above, both nasal tract lesions (upper 
respiratory effects) and neurologic effects are chronic effects of 
concern. These effects occur in a clear dose concentration manner with 
the lowest levels of hydrogen sulfide exposure associated with these 
effects ranging from 20 to 30 ppm (28 mg/m\3\ to 41.7 mg/m\3\).

B. What Is EPA's Evaluation of the Environmental Toxicity of Hydrogen 
Sulfide?

    A number of ecotoxicity studies have been conducted on hydrogen 
sulfide, mainly on freshwater invertebrates and fish. Acute, chronic, 
and early-life stage toxicity values for hydrogen sulfide include 
numerous values that are well below 1 milligram per liter (mg/L), 
indicating that hydrogen sulfide is toxic at very low concentrations. 
EPA's ecological assessment (Ref. 2) includes an extensive listing of 
the aquatic toxicity values for hydrogen sulfide. Some examples of the 
values from Table 2-1 of EPA's ecological assessment (Ref. 2) are 
provided below.
    Hydrogen sulfide acute toxicity values (96-hour LC50 
(i.e., the concentration that is lethal to 50% of test organisms)) for 
freshwater fish ranged from 0.0149 mg/L (fathead minnow) to 0.0448 mg/L 
(bluegill). Chronic toxicity values for freshwater fish ranged from a 
6-week lowest-observed-effect-concentration (LOEC) (growth rate) of 
0.0005 mg/L in a tropical fish (Mystus nemurus) to a 430-day LOEC 
(final weight) of 0.009 mg/L for goldfish. Additionally, in early-life 
stage toxicity testing with eggs, fry, and juveniles of various 
freshwater fish species, endpoint values ranged from a 96-hour 
LC50 of L (yellow perch sac fry) to a 96-hour 
LC50 value of 0.0536 mg/L (fathead minnow). The hydrogen 
sulfide 96-hour LC50 values for freshwater invertebrates 
ranged from 0.021 mg/L (amphipod) to 1.07 mg/L (isopod), and 48- to 96-
hour LC50 values for estuarine/marine invertebrates ranged 
from 0.063 mg/L (saltwater shrimp) to 0.332 mg/L (adult amphipod). The 
hydrogen sulfide EC50 (i.e., the concentration that is 
effective in producing a sublethal response in 50% of test organisms) 
values for estuarine/marine invertebrates included 0.01 mg/L (saltwater 
mussel) and 0.019 mg/L (sea urchin). Hydrogen sulfide chronic values 
for freshwater invertebrates ranged from a 65-day LOEC (reproduction) 
of 0.0031 mg/L to a 10-day LC50 value of 0.042 mg/L, both 
for the amphipod Gammarus pseudolimnaeus. For early-life stage toxicity 
testing, a 96-hour LC50 value of 0.034 mg/L was available 
for juvenile crayfish (freshwater species), and for estuarine/marine 
invertebrates, 48-hour LC50 values of 0.0087 mg/L and 0.0185 
mg/L were available for white shrimp larvae and juveniles, 
respectively.

V. EPA's Use of Exposure Analyses

    The Agency's position on the use of exposure analyses in listing 
decisions under EPCRA section 313 was presented in a proposed rule in 
the Federal Register of January 12, 1994 (59 FR 1788). The proposed 
rule provided the public with the opportunity to comment on the 
Agency's interpretation of the statutory listing criteria as it relates 
to the use of exposure considerations. After considering the comments 
received, EPA published in the Federal Register of November 30, 1994 
(59 FR 61432) a statement clarifying its interpretation of the 
statutory requirements regarding how exposure will be considered in 
listing decisions. Subsequent to the final rule, EPA's interpretation 
of the statutory listing criteria as it relates to the consideration of 
exposure was upheld in National Oilseed Processors Ass'n. v. Browner, 
924 F. Supp. 1193 (D.D.C. 1996), aff'd in part & remanded in part, Troy 
Corp. v. Browner, 120 F.3d 277 (D.C. Cir. 1997).
    EPA has determined that hydrogen sulfide can reasonably be 
anticipated to cause serious or irreversible chronic human health 
effects at relatively low doses and thus is considered to have 
moderately high to high chronic toxicity. EPA does not believe that it 
is appropriate to consider exposure for chemicals that are moderately 
high to highly toxic based on a hazard assessment when determining if a 
chemical can be listed for chronic effects pursuant to EPCRA section 
313(d)(2)(B) (see 59 FR 61432, 61433, 61440-61442). Hydrogen sulfide 
has also been determined to cause ecotoxicity at relatively low 
concentrations, and thus is considered to have high ecotoxicity. EPA 
believes that chemicals that induce death or serious adverse effects in 
aquatic organisms at relatively low concentrations (i.e., they have 
high ecotoxicity) have the potential to cause significant changes in 
the population of fish and other aquatic organisms, and can therefore 
reasonably be anticipated to cause a significant adverse effect on the 
environment of sufficient seriousness to warrant reporting. EPA does 
not believe that it is required to consider exposure for chemicals that 
have high ecotoxicity based on a hazard assessment when determining if 
a chemical can be listed for effects pursuant to EPCRA section 
313(d)(2)(C) (see 59 FR 61432, 61433, 61440-61442).

VI. What Is EPA's Rationale That the Administrative Stay Should Be 
Lifted?

    EPA's technical evaluation of hydrogen sulfide shows that it can 
reasonably be anticipated to cause chronic health effects in humans. 
The chronic health effects have been observed in laboratory animals at 
concentrations as low as 28 mg/m\3\ (20 ppm) and 41.7 mg/m\3\ (30 ppm). 
In addition, EPA's technical evaluation of hydrogen sulfide also shows 
that it can reasonably be anticipated to cause, because of its 
toxicity, significant adverse effects in aquatic organisms. Examples of 
hydrogen sulfide's ecological toxicity include acute toxicity (96-hour 
LC50) values for freshwater fish that ranged from 0.0149 mg/
L (fathead minnow) to 0.0448 mg/L (bluegill), indicating high aquatic 
toxicity. Examples of hydrogen sulfide's chronic ecological toxicity 
include freshwater fish values that ranged from a 6-week LOEC (growth 
rate) of 0.0005 mg/L in a tropical fish (Mystus nemurus) to a 430-day 
LOEC (final weight) of 0.009 mg/L for goldfish, also indicating high 
aquatic toxicity.
    Based on the above findings, EPA believes that there is no basis 
for continuing the Administrative Stay of the reporting requirements 
for hydrogen sulfide, and that the Administrative Stay should therefore 
be lifted. As an aside, EPA notes also that it believes that the above 
findings clearly demonstrate the correctness of the Agency's final 
decision in December 1993 to list hydrogen sulfide on the EPCRA section 
313 toxic chemicals list

[[Page 8894]]

based on the listing criteria in EPCRA sections 313(d)(2)(B) and (C).
    Finally, in accordance with EPA's stated policy on the use of 
exposure assessments (59 FR 61432), EPA does not believe that an 
exposure assessment is appropriate for determining whether hydrogen 
sulfide meets the criteria of EPCRA section 313(d)(2)(B) or (C), and 
therefore the Administrative Stay should not be continued for lack of 
an exposure analysis.

VII. What Are the References Cited in This Document?

    EPA has established an official public docket for this action under 
Docket ID No. EPA-HQ-TRI-2009-0844. The public docket includes 
information considered by EPA in developing this action, including the 
documents listed below, which are electronically or physically located 
in the docket. In addition, interested parties should consult documents 
that are referenced in the documents that EPA has placed in the docket, 
regardless of whether these referenced documents are electronically or 
physically located in the docket. For assistance in locating documents 
that are referenced in documents that EPA has placed in the docket, but 
that are not electronically or physically located in the docket, please 
consult the person listed in the above FOR FURTHER INFORMATION CONTACT 
section.

    1. U.S. Environmental Protection Agency. ``Toxicological Review 
of Hydrogen sulfide, (CAS No. 7783-06-4), In Support of Summary 
Information on the Integrated Risk Information System.'' Washington, 
DC: Integrated Risk Information System. U.S. Environmental 
Protection Agency. June, 2003. http://www.epa.gov/ncea/iris/toxreviews/0061-tr.pdf Integrated Risk Information Summary for 
Hydrogen Sulfide available at: http://www.epa.gov/ncea/iris/subst/0061.htm.
    2. U.S. Environmental Protection Agency, Technical Review of 
Hydrogen Sulfide: Chemistry, Environmental Fate and Ecological 
Toxicity, CAS Registry Number 7783-06-4; Office of Environmental 
Information, Office of Information Access and Analysis, 
Environmental Analysis Division, Analytical Support Branch; June 22, 
2009.
    3. Tvedt, B., Edland, A., Skyberg, K. et al., ``Delayed 
neuropsychiatric sequelae after acute hydrogen sulfide poisoning: 
affection of motor function, memory, vision and hearing.'' Acta. 
Neurol. Scand. v. 84, (1991), pp. 348-351.
    4. Tvedt, B., Skyberg, K., Aaserud, O., et al., ``Brain damage 
caused by hydrogen sulfide: a follow-up study of six patients.'' Am. 
J. Ind. Med. v. 20, (1991), pp. 91-101.
    5. Wasch, H.H., Estrin, W.J., Yip, P. et al., ``Prolongation of 
the P-300 latency associated with hydrogen sulfide exposure.'' Arch. 
Neurol. v. 46, (1989), pp. 902-904.
    6. Brenneman, K.A., James, R.A., Gross, E.A., Dorman, D.C., 
``Olfactory neuron loss in adult male CD rats following subchronic 
inhalation exposure to hydrogen sulfide.'' Toxicol. Pathol. v. 
28(2), (2000), pp. 326-333.
    7. Hannah, R.S., Roth, S.H., ``Chronic exposure to low 
concentrations of hydrogen sulfide produces abnormal growth in 
developing Purkinje cells.'' Neurosci. Lett. v. 122, (1991), pp. 
225-228.
    8. Dorman, D.C., Brenneman, K.A., Struve, M.F., et al., (2000) 
``Fertility and developmental neurotoxicity effects of inhaled 
hydrogen sulfide in Sprague-Dawley rats.'' Neurotoxicol Teratol. v. 
22, (2000), pp. 71-84.
    9. Chemical Industry Institute of Toxicology, ``90-Day vapor 
inhalation toxicity study of hydrogen sulfide in B6C3F1 mice.'' 
(1983), EPA/OTS 0883-0255.
    10. Lopez, A., Prior, M., Yong, S., et al., ``Nasal lesions in 
rats exposed to hydrogen sulfide for four hours.'' Am. J. Vet. Res. 
v. 49(7), (1988), pp. 1107-1111.
    11. Dorman, D.C., Struve, M.F., Gross, E.A., et al., 
``Respiratory tract toxicity of inhaled hydrogen sulfide in Fischer-
344 rats, Sprague-Dawley rats, and B6C3F1 mice following subchronic 
(90-day) exposure.'' Toxicol Appl Pharmacol v. 198, (2004), pp. 29-
39.
    12. Hirsch, A.R., Zavala, G., ``Long-term effect on the 
olfactory system of exposure to hydrogen sulphide.'' Occup. Environ. 
Med. v. 56, (1999), pp. 284-287.
    13. Chemical Industry Institute of Toxicology, ``90-Day vapor 
inhalation toxicity study of hydrogen sulfide in Fischer-344 rats.'' 
(1983), EPA/OTS 0883-0255.
    14. Chemical Industry Institute of Toxicology, ``90-Day vapor 
inhalation toxicity study of hydrogen sulfide in Sprague-Dawley 
rats.'' (1983), EPA/OTS 0883-0255.
    15. Skrajny, B., Hannah, R.S., Roth, S.H., ``Low concentrations 
of hydrogen sulphide alter monoamine levels in the developing rat 
central nervous system.'' Can. J. Physiol. Pharmacol. v. 70(11), 
(1992), pp. 1515-1518.
    16. Hannah, R.S., Hayden, L.J., Roth, S.H., ``Hydrogen sulfide 
exposure alters the amino acid content in developing rat CNS.'' 
Neurosci. Lett. v. 99, (1989), pp. 323-327.
    17. Hannah, R.S., Bennington, R., Roth, S.H., ``A relationship 
between hydrogen sulfide exposure and taurine levels in maternal 
rats.'' Proc West Pharmacol Soc v. 33, (1990), pp. 177-179.
    18. U.S. Environmental Protection Agency, ``Guidelines for 
neurotoxicity risk assessment.'' Federal Register, May 14, 1998, 
63(93):26926-26954. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=12479

List of Subjects in 40 CFR Part 372

    Environmental protection, Community right-to-know, Reporting and 
recordkeeping requirements, and Toxic chemicals.

    Dated: February 19, 2010.
Lisa P. Jackson,
Administrator.
[FR Doc. 2010-4084 Filed 2-25-10; 8:45 am]
BILLING CODE 6560-50-P
```